| Abstrakt: |
It has been reported previously that Δ-tetrahydrocannabinol and the synthetic cannabinoid agonist HU-210 [(−)-11-OH-Δ-dimethylheptyl tetrahydrocannabinol] prevent long-term potentiation (LTP) induction in rat hippocampal slices. In this study we confirm that both WIN55212-2 {R-(+)-(2,3-dihydro-5-methyl-3-[{4-morpholinyl} methyl] pyrol [1,2,3-de]-1,4-benzoxazin-6-yl) (1-naphtalenyl) methanone monomethanesulphonate} (3 and 10 μM), another synthetic cannabinoid agonist, and anandamide (10 μM), considered to be the endogenous ligand of cannabinoid receptors, inhibit LTP formation in the Schaffer collateral-CA1 field complex. In addition, we show that SRt417l6A [ N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2, 4-dichlorophenyl)-4-methyl-lH-pyrazole-3-carboxamide hydrochloride] at 0.1-10 μM, a potent and selective antagonist of CB1 cannabinoid receptors, concentration-dependently reversed the inhibition of LTP induced by both WIN55212-2 and anandamide. These data indicate that cannabinoid receptor agonists inhibit hippocampal LTP formation through CB1 receptor activation and that anandamide could be a candidate for an endogenous neuromessenger involved in memory processes. [ABSTRACT FROM AUTHOR] |
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